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Abstract
Thyrotoxicosis is associated with an increase in cardiac work and in experimental animals leads to the development of cardiac hypertrophy (1,2). Thyroid hormone (T4) exerts its biologic activity by binding to discrete nuclear receptors, with the subsequent alteration in the rate of RNA transcription leading to the synthesis of specific proteins (3). Previous studies have suggested that increases in cardiac protein synthesis and cardiac contractility can be a result of a direct effect of thyroid hormone on the heart (1,2,4). In various models of cardiac hypertrophy produced by an increase in cardiac work there is a similar rapid increase in both RNA and protein synthesis (5). Thus it is possible that the development of cardiac hypertrophy in hyperthyroidism is due to either a direct effect of thyroid hormone on the heart or alternatively is a response of the myocardium to an increase in cardiac work.
Published Version
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